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A salt-regulated peptide derived from the CAP superfamily protein negatively regulates salt-stress tolerance in Arabidopsis.

Chien PS, Nam HG, Chen YR - J. Exp. Bot. (2015)

Bottom Line: This peptide was found by searching homologues in Arabidopsis using the precursor of a tomato CAP-derived peptide (CAPE) that was initially identified as an immune signal.In searching for a CAPE involved in salt responses, we screened CAPE precursor genes that showed salt-responsive expression and found that the PROAtCAPE1 (AT4G33730) gene was regulated by salinity.We confirmed the endogenous Arabidopsis CAP-derived peptide 1 (AtCAPE1) by mass spectrometry and found that a key amino acid residue in PROAtCAPE1 is critical for AtCAPE1 production.

View Article: PubMed Central - PubMed

Affiliation: Molecular and Biological Agricultural Sciences Program, Taiwan International Graduate Program, Academia Sinica, Taipei 115, Taiwan Agricultural Biotechnology Research Center, Academia Sinica, Taipei 115, Taiwan Graduate Institute of Biotechnology, National Chung-Hsing University, Taichung 402, Taiwan.

No MeSH data available.


Related in: MedlinePlus

Number of genes differentially expressed in wild type (Ler) and the proatcape1 mutant under high salt. (A) Numbers indicate the genes with significantly differential expression (P≤0.05 and a greater than 1.5-fold change) between the indicated data sets derived from microarray analysis. (B) Number of genes with differential expression levels between wild type and the proatcape1 mutant under normal and salt (12h of treatment in 125mM NaCl) conditions (P≤0.05 and a greater than 1.5-fold change).
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Figure 4: Number of genes differentially expressed in wild type (Ler) and the proatcape1 mutant under high salt. (A) Numbers indicate the genes with significantly differential expression (P≤0.05 and a greater than 1.5-fold change) between the indicated data sets derived from microarray analysis. (B) Number of genes with differential expression levels between wild type and the proatcape1 mutant under normal and salt (12h of treatment in 125mM NaCl) conditions (P≤0.05 and a greater than 1.5-fold change).

Mentions: To gain insight into the mechanism by which AtCAPE1 regulates salt responses, we investigated the gene expression profiles of wild-type (Ler) and proatcape1 mutant seedlings in the presence and absence of 125mM NaCl by microarray analysis (Fig. 4). First, we identified 3495 and 4412 genes that were up- and downregulated, respectively, by over 1.5-fold in the wild type after 12h of treatment in 125mM NaCl (Fig. 4A; Supplementary dataset I, available at JXB online). This observation was in agreement with previous reports that salt treatment leads to a large change in the gene expression profile and is involved in many physiological processes (Kreps et al., 2002; Seki et al., 2002; Jiang and Deyholos, 2006). In the mutant, 3975 and 5284 genes were up- and downregulated, respectively, by over 1.5-fold under salinity (Fig. 4A; Supplementary dataset II, available at JXB online). The result showed that the overall sensitivity of plants to salt stress was increased in the mutant, as more genes were affected in the mutant than in the wild type. We then compared the genes that were differentially expressed in the wild type and mutant. Under normal conditions, 245 and 292 genes were up- and downregulated by over 1.5-fold in the mutants (Fig. 4B; Supplementary dataset III, available at JXB online). In contrast, after 12h of treatment with 125mM NaCl, 587 and 378 genes were up- and downregulated by over 1.5-fold in the mutants (Fig. 4B; Supplementary dataset IV, available at JXB online). The result showed that more genes were upregulated under high salinity. As the mutant displayed salt tolerance, it is likely that these upregulated genes in the mutant under high salinity contribute to the salt-tolerant phenotype. As analysed by Gene Ontology (GO) (Huang et al., 2009a, b), the gene products of these genes could be described by GO terms including ‘response to water deprivation’, ‘response to abscisic acid stimulus’, and ‘response to salt stress’ (Table 2).


A salt-regulated peptide derived from the CAP superfamily protein negatively regulates salt-stress tolerance in Arabidopsis.

Chien PS, Nam HG, Chen YR - J. Exp. Bot. (2015)

Number of genes differentially expressed in wild type (Ler) and the proatcape1 mutant under high salt. (A) Numbers indicate the genes with significantly differential expression (P≤0.05 and a greater than 1.5-fold change) between the indicated data sets derived from microarray analysis. (B) Number of genes with differential expression levels between wild type and the proatcape1 mutant under normal and salt (12h of treatment in 125mM NaCl) conditions (P≤0.05 and a greater than 1.5-fold change).
© Copyright Policy - creative-commons
Related In: Results  -  Collection

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Figure 4: Number of genes differentially expressed in wild type (Ler) and the proatcape1 mutant under high salt. (A) Numbers indicate the genes with significantly differential expression (P≤0.05 and a greater than 1.5-fold change) between the indicated data sets derived from microarray analysis. (B) Number of genes with differential expression levels between wild type and the proatcape1 mutant under normal and salt (12h of treatment in 125mM NaCl) conditions (P≤0.05 and a greater than 1.5-fold change).
Mentions: To gain insight into the mechanism by which AtCAPE1 regulates salt responses, we investigated the gene expression profiles of wild-type (Ler) and proatcape1 mutant seedlings in the presence and absence of 125mM NaCl by microarray analysis (Fig. 4). First, we identified 3495 and 4412 genes that were up- and downregulated, respectively, by over 1.5-fold in the wild type after 12h of treatment in 125mM NaCl (Fig. 4A; Supplementary dataset I, available at JXB online). This observation was in agreement with previous reports that salt treatment leads to a large change in the gene expression profile and is involved in many physiological processes (Kreps et al., 2002; Seki et al., 2002; Jiang and Deyholos, 2006). In the mutant, 3975 and 5284 genes were up- and downregulated, respectively, by over 1.5-fold under salinity (Fig. 4A; Supplementary dataset II, available at JXB online). The result showed that the overall sensitivity of plants to salt stress was increased in the mutant, as more genes were affected in the mutant than in the wild type. We then compared the genes that were differentially expressed in the wild type and mutant. Under normal conditions, 245 and 292 genes were up- and downregulated by over 1.5-fold in the mutants (Fig. 4B; Supplementary dataset III, available at JXB online). In contrast, after 12h of treatment with 125mM NaCl, 587 and 378 genes were up- and downregulated by over 1.5-fold in the mutants (Fig. 4B; Supplementary dataset IV, available at JXB online). The result showed that more genes were upregulated under high salinity. As the mutant displayed salt tolerance, it is likely that these upregulated genes in the mutant under high salinity contribute to the salt-tolerant phenotype. As analysed by Gene Ontology (GO) (Huang et al., 2009a, b), the gene products of these genes could be described by GO terms including ‘response to water deprivation’, ‘response to abscisic acid stimulus’, and ‘response to salt stress’ (Table 2).

Bottom Line: This peptide was found by searching homologues in Arabidopsis using the precursor of a tomato CAP-derived peptide (CAPE) that was initially identified as an immune signal.In searching for a CAPE involved in salt responses, we screened CAPE precursor genes that showed salt-responsive expression and found that the PROAtCAPE1 (AT4G33730) gene was regulated by salinity.We confirmed the endogenous Arabidopsis CAP-derived peptide 1 (AtCAPE1) by mass spectrometry and found that a key amino acid residue in PROAtCAPE1 is critical for AtCAPE1 production.

View Article: PubMed Central - PubMed

Affiliation: Molecular and Biological Agricultural Sciences Program, Taiwan International Graduate Program, Academia Sinica, Taipei 115, Taiwan Agricultural Biotechnology Research Center, Academia Sinica, Taipei 115, Taiwan Graduate Institute of Biotechnology, National Chung-Hsing University, Taichung 402, Taiwan.

No MeSH data available.


Related in: MedlinePlus